Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The characteristics of thyroglobulin (Tg) autoantibodies in Obese strain (OS) chickens with thyroiditis have been defined and compared with those of polyclonal antibodies to chicken Tg produced by immunizing normal chickens and a rabbit, and with mouse monoclonal antibodies (MoAb) to chicken Tg. Chicken Tg autoantibodies (aAb), when tested against Tg from 24 species all showed specificity for chicken Tg which ranged from absolute to limited although in most instances cross-reactions with Tgs of other species were either absent or at a low level. Antibodies to chicken Tg produced by immunization showed a similar limited range of cross-reactions. Four of five chTg-MoAbs were specific for chicken Tg and the fifth was almost so. In competitive experiments, the polyclonal rabbit antibody could fully inhibit binding of all chicken Tg-aAb to chicken Tg but not vice versa. It was inferred that polyclonal rabbit Tg antiserum includes antibodies to all the epitopes seen by chicken Tg-aAb and many more besides. In similar experiments with four chicken Tg-MoAbs, the binding of one chicken Tg-aAb was unaffected, and three other patterns of inhibitions were defined. The binding to chicken Tg of a fifth chicken Tg-MoAb was enhanced rather than inhibited by chicken Tg-aAb. Some but not all chicken Tg-aAb preparations could differentiate between Tgs containing different amounts of thyroxine. We conclude that the autoantibodies to Tg in OS chickens are directed in the main against determinants unique to the species. Not all the species-specific determinants are involved in the autoimmune response but the number of epitopes involved is at least four. In these respects the immune response to Tg in OS chickens resembles that in autoimmune thyroid disease in humans. The conformation of chicken Tg may be affected by combination with antibody or by the content of thyroid hormone.
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PMID:Selective autoimmune response to the chicken-specific structures of thyroglobulin in Obese strain chickens. 276 75

Two cases are reported of women aged 18 and 36 years respectively who developed a typical picture of hyperthyroidism by Graves Basedow disease (primary hyperthyroidism, diffuse goiter with increased uptake, positive stimulating thyroid antibodies, exophthalmos). These women had taken drugs for obesity which were prepared by magistral formula and acquired by mail 8 and 9 months prior to diagnosis of the disease. The differential diagnosis is discussed which should be considered in a women with hyperthyroidism and the antecedent of ingestion of weight-reducer drugs as well as the orientative data of the different causes. Also, the possible role of these drugs as triggering factor for the autoimmune thyroid disease is discussed.
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PMID:[Graves Basedow disease following treatment with magistral formulae for obesity. Jod-Basedow phenomenon?]. 941 56

Almost all major causes of ill-health and premature death in human societies worldwide - including cancer, cardiovascular disease, diabetes and many infectious diseases - are, at least in part, genetically determined. Typically, risk of succumbing to one of these illnesses is thought to depend on both the individual repertoire of variation within a number of key susceptibility genes and the history of exposure to relevant environmental factors. For many of these conditions, the molecular basis of disease pathogenesis remains obscure. This represents a major obstacle to development of improved, rational strategies for disease treatment, prevention and eradication. It is easy therefore to appreciate the importance attached to efforts to deliver more comprehensive understanding of the molecular basis of disease pathogenesis. Nor is it hard to understand that identification of major susceptibility genes should highlight those components of molecular machinery that are critical for the preservation of normal health. The benefits promised are great, but progress to gene identification in multifactorial traits has been rather disappointing to date. Why is this? This review aims to answer this question by describing current and future approaches to gene discovery in multifactorial traits. The examples quoted will mostly relate to type 2 diabetes, but the issues and approaches are generic, and apply equally to other multifactorial traits in the endocrine and metabolic arena - type 1 diabetes; obesity; hyperlipidaemia; autoimmune thyroid disease; polycystic ovarian syndrome - and beyond.
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PMID:Susceptibility gene discovery for common metabolic and endocrine traits. 1185 95

The proband, a 9-year-old Hispanic female, presented with hair loss, strabismus, and weight gain. On magnetic resonance imaging (MRI) she was found to have severe primary hypothyroidism and a large pituitary mass. In addition, acanthosis nigricans, obesity, and hyperinsulinism were observed. Findings were similar in three of four siblings. Thyroid peroxidase antibodies were detected in the father and three of four siblings. Although all family members were obese, and hyperinsulinemia with high proinsulin and C-peptide was found in all except one sibling, only the mother and one child had overt type 2 diabetes mellitus. Because of the unusual association of autoimmune thyroid disease, insulin resistance and obesity rather than insulin deficiency, we searched for possible genetic abnormalities. The HLA haplotypes did not cosegregate with autoimmune thyroid disease or insulin resistance. Mutational analysis of known obesity genes was done. Leptin was not deficient, and sequencing of the proband's DNA showed no mutations in the perixisome proliferator activated receptor (PPAR)-gamma, PPAR-gamma(2), PPAR-alpha or melanocortin 4 receptor genes. Maternally inherited diabetes and deafness was ruled out since no mutations were found in mitochondria DNA. Insulin receptor antibodies were not detected. In conclusion, the remarkably high incidence of childhood autoimmune hypothyroidism, pituitary enlargement, insulin resistance and obesity in this family is not linked to known HLA types or known gene defects.
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PMID:Familial juvenile autoimmune hypothyroidism, pituitary enlargement, obesity, and insulin resistance. 1514 66

Twins are two independent babies delivered during the same pregnancy and are divided as monozygotic or dizygotic based on their origin. Dizygotic twins are similar to two siblings and have different genetic information. In contrary, monozygotic twins have a similar genetic identity and provide a unique opportunity to evaluate the contribution of genetic and environmental factors of the disease. The endocrine and metabolic disorders affect a large number of the population including the twins. Diabetes, obesity, and autoimmune thyroid disease are the most common endocrine disorders in general practice. It is essential to understand the genetic basis of endocrine disorders for therapy, prognostication and risk assessment for future generations. In this article, we review the endocrine disorders in relation to their occurrence in monozygotic twins to highlight the genetic and environmental contribution.
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PMID:Twins and endocrinology. 2553 77

As the prevalence of these endocrine dysfunctions increases, the association of polycystic ovary syndrome (PCOS) and autoimmune thyroid disease is increasingly being recognised. While the causality of this association is still uncertain, the two conditions share a bidirectional relationship. The exact nature of this link has not been elucidated yet. Both syndromes share certain common characteristics, risk factors, and pathophysiological abnormalities. Simultaneously, certain etiopathogenetic factors that operate to create these dysfunctions are dissimilar. Polycystic appearing ovaries are a clinical feature of hypothyroidism, though hypothyroidism should be excluded before diagnosing PCOS. Adiposity, increased insulin resistance, high leptin, evidence of deranged autoimmunity, all of which are present in both disease states, seem to play a complex role in connecting these two disorders. This brief communication explores the nature of the relationship between PCOS and hypothyroidism. It reviews current data and analyses them to present a unified pathophysiological basis, incorporating these complex relationships, for the same.
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PMID:Thyroid disorders and polycystic ovary syndrome: An emerging relationship. 2559 22

Obesity-related changes in the composition of the body interfere with the proper functioning of the thyrotropic axis, leading to its disturbances and changes in the structure of the thyroid gland. Distinguishing what is related to obesity and what constitutes pathological changes is crucial for the proper treatment of patients. In this paper authors present a case of a patient with a diet-induced obesity, whose only abnormalities in thyroid assessment included an elevated level of thyroid stimulating hormone (TSH) and hypoechoic thyroid gland on ultrasound. Based on this clinical situation, we reviewed literature in order to establish rules regarding management of thyroid disorders in obese individuals. The most common obesity-related thyroid abnormality is an isolated increase of TSH, without clinical symptoms of hypothyroidism, defined as hyperthyrotropinaemia. In obese adults, autoimmune thyroid disease is found equally often as in the normal-weight population. Thyroid enlargement, increased risk of nodules, and decreased echogenicity, not related to autoimmunity, is frequent among obese individuals. Weight loss leads to the normalisation of TSH levels and thyroid echogenicity. Excessive weight can influence both the TSH level and ultrasound image of the thyroid gland; however, these findings can be reversed by weight reduction. Therefore, in asymptomatic obese patients elevated TSH should not be treated with thyroid hormone replacement.
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PMID:Diagnosis and treatment of thyroid disorders in obese patients - what do we know? 3129 May 58